Multihormonal Regulation of Hepatic Histidase during Postnatal Development

Abstract

Hepatic histidase of the rat is presented as a model system, wherein multihormonal regulation, effecting a complex postnatal developmental course of an enzyme level, is explored. Three hormonal inducers of rat liver histidase: estrogen, glucocorticoid and glucagon, and several suppressors of this enzyme: pituitary products (including growth hormone and ACTH) and thyroxine, participate in the regulation of the postnatal development of this enzyme. The developmental pattern of competence of the liver to respond to each hormonal inducer is temporally characteristic for each hormone: estrogen being capable of inducing histidase only in animals beyond the neonatal stage, glucocorticoid of inducing the enzyme only during the first two postnatal months, and glucagon being a functional inducer at all postnatal stages. Estrogen is responsible for the rise in histidase levels associated with the female during puberty, glucagon, via cyclic AMP, participates in implementing the neonatal rise in the enzyme; and glucocorticoid is a requirement for both the neonatal and male adolescent elevations of this enzyme. A network of interplay among the hormones is revealed, in which the pituitary is required to mediate estrogenic induction and androgen and the two inducers, glucocorticoid and glucagon, curtail estrogenic induction. Transcriptional and translational processes have been implicated as underlying all the hormonal influences on histidase studied and the normal adolescent developmental rise of the enzyme. It is thus concluded that the complex postnatal developmental course of hepatic histidase is shaped by the resultant of a temporally determined interplay of a variety of stimulatory and suppressive endocrine influences.

Endocrine regulation of sex differences in hepatic histidase activity

“…From birth through the early part ofthe pre-pubertal period, hepatic histidase activities are similar in male and female rats, but, beginning at puberty and extending into adulthood, histidase activities are higher in adult females than in adult males (Feigelson, 1973). Oestrogen is a positive modulator, whereas testosterone is a negative effector, of histidase (Feigelson, 1973). In intact animals, glucocorticoids, glucagon via cyclic AMP, and amino acids (Feigelson, 1973) and growth hormone (somatotropin) (Skett & Gustafsson, 1979), result in increased activity.…”

“…The endocrine regulation of hepatic histidase is mediated via the hypothalamic-hypophyseal-gonadal axis. From birth through the early part ofthe pre-pubertal period, hepatic histidase activities are similar in male and female rats, but, beginning at puberty and extending into adulthood, histidase activities are higher in adult females than in adult males (Feigelson, 1973). Oestrogen is a positive modulator, whereas testosterone is a negative effector, of histidase (Feigelson, 1973).…”

“…Oestrogen is a positive modulator, whereas testosterone is a negative effector, of histidase (Feigelson, 1973). In intact animals, glucocorticoids, glucagon via cyclic AMP, and amino acids (Feigelson, 1973) and growth hormone (somatotropin) (Skett & Gustafsson, 1979), result in increased activity. The thyroid is suppressive to the expression of histidase (Freedland et al, 1968; Armstrong & Feigelson, 1980).…”

Immunological Relationships among Fungal and Plant Phenylalanine Ammonia-lyases and Bacterial Histidine Ammonia-lyase

“…대사 적으로는 shikimic acid 경로를 통해 생성된 phenylalanine을 리그닌, 슈베린, 플라보노이드, 안토시아닌, 탄닌, 파이토알렉 신 등 매우 다양한 phenylpropane 계 2차 대사물질을 만드는 대사의 초기에 작용하는 효소이다 (Hahlbrock와 Scheel, 1989). 식물에 비하여 곰팡이에 있어서는 PAL에 대한 연구가 매우 미진하여 몇몇 곰팡이 종에 한정된 연구보고만 있는 실 정이다 (Schomburg and Salzmann, 1990 (Hollman and Dekker, 1971;Polkinghorne and Hynes, 1982)과 식물 Kindl, 1970 and1971;Kamel and Maksoud, 1978) (Feigelson, 1973;Lamartiniere, 1979;Armstrong and Feigelson, 1980).…”

Role of Thyroxine in the Postnatal Development of Rat Hepatic Tryptophan Oxygenase and Ornithine Aminotransferase

“…The possibility of a role for thyroxine in the ontogenic increases of tryptophan oxygenase and ornithine aminotransfer-ase activity has not been previously investigated. Exogenous thyroid hormone and glucocorticoids have opposing effects on the natural rise of hepatic histidase development (9,10) and hepatic hexosaminidase (12). Thus, four possibilities exist for the role of thyroxine in the development of hepatic tryptophan oxygenase and ornithine aminotransferase in the late suckling period: (i) a permissive role mediated by glucocorticoids; (ii) a role synergistic with corticosterone; (iii) a role independent of glucocorticoids (negative or additive); or (iv) no effect.…”